Syncope Joseph P. Ornato, MD, FACP, FACC, FACEP

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Presentation transcript:

Syncope Joseph P. Ornato, MD, FACP, FACC, FACEP Professor & Chairman, Department of Emergency Medicine

Syncope – A symptom, not a diagnosis Self-limited loss of consciousness and postural tone Relatively rapid onset Variable warning symptoms Spontaneous, complete, and usually prompt recovery without medical or surgical intervention Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537. Underlying mechanism is transient global cerebral hypoperfusion. Brignole M, et al. Europace, 2004;6:467-537.

Classification of Transient Loss of Consciousness (TLOC) Real or Apparent TLOC Syncope Neurally-mediated reflex syndromes Orthostatic hypotension Cardiac arrhythmias Structural cardiovascular disease Disorders Mimicking Syncope With loss of consciousness (i.e., seizure disorders, concussion) Without loss of consciousness, i.e., psychogenic “pseudo-syncope” Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537. Brignole M, et al. Europace, 2004;6:467-537.

Unexplained Causes = Approximately 1/3 Causes of true syncope Orthostatic Cardiac Arrhythmia Structural Cardio- Pulmonary 1 Vasovagal syndrome Carotid sinus syndrome • Situational Cough Post- Micturition 2 Drug-induced • Autonomic nervous system failure Primary Secondary 3 Bradyarrhythmia Sinus node dysfunction AV block •Tachyarrhythmia VT SVT Long QT syndrome 4 Acute myocardial ischemia Aortic stenosis Hypertrophic cardiomyopathy Pulmonary hypertension Aortic dissection Neurally- Mediated Unexplained Causes = Approximately 1/3 This slide provides a simple classification of the principal causes of syncope, listed from the most commonly observed (left) to the least common (right). This ranking may be helpful in thinking about the strategy for evaluating syncope in individual patients. Within the boxes, the most common causes of syncope are indicated for each of the major diagnostic groups. The terms ‘neurally-mediated syncope’, ‘neurally-mediated reflex syncope,’ and ‘neurocardiogenic syncope’ are generally used synonymously. For purposes of this presentation, ‘neurally-mediated syncope’ is used to define a broad category; ‘neurocardiogenic’ or ‘vasovagal syncope’ refer to a specific condition. VVS—Vasovagal Syncope CSS—Carotid Sinus Syndrome ANS—Autonomic Nervous System HCM—Hypertrophic Cardiomyopathy DG Benditt, MD. University of Minnesota Cardiac Arrhythmia Center

Syncope mimics Acute intoxication (e.g., alcohol) Seizures Sleep disorders Somatization disorder (psychogenic pseudo-syncope) Trauma/concussion Hypoglycemia Hyperventilation Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537. Brignole M, et al. Europace, 2004;6:467-537.

Impact of syncope 40% will experience syncope at least once in a lifetime1 1-6% of hospital admissions2 1% of emergency department visits per year3,4 10% of falls by elderly are due to syncope5 Major morbidity reported in 6%1 (fractures, motor vehicle crashes) Minor injury in 29%1 (lacerations, bruises) 1Kenny RA, Kapoor WN. Epidemiology and social costs. In: Benditt D, Blanc J-J, et al. eds. The Evaluation and Treatment of Syncope. Elmsford, NY: Futura;2003:23-27. 2Kapoor W. Evaluation and outcome of patients with syncope. Medicine. 1990;69:160-175. 3Brignole M, Disertori M, Menozzi C, et al. Management of syncope referred urgently to general hospitals with and without syncope units. Europace. 2003;5:293-298. 4 Blanc J-J, L’ Her C, Touiza A, et al. Prospective evaluation and outcome of patients admitted for syncope over a 1 year period. Eur Heart J. 2002;23:815-820. 5Campbell A, Reinken J, Allan B, et al. Falls in old age: A study of frequency and related clinical factors. Age and Ageing. 1981;10:264-270. 1Kenny RA, Kapoor WN. In: Benditt D, et al. eds. The Evaluation and Treatment of Syncope. Futura;2003:23-27. 2Kapoor W. Medicine. 1990;69:160-175. 3Brignole M, et al. Europace. 2003;5:293-298. 4 Blanc J-J, et al. Eur Heart J. 2002;23:815-820. 5Campbell A, et al. Age and Ageing. 1981;10:264-270.

Impact of syncope: costs Estimated hospital costs exceeded $10 billion1 Estimated physician office expenses exceeded $470 million2 Over $7 billion is spent annually in the US to treat falls in older adults4 1Kenny RA, Kapoor WN. Epidemiology and social costs. In: Benditt D, Blanc J-J, et al. eds. The Evaluation and Treatment of Syncope. Elmsford, NY: Futura;2003:23-27. 2 Solucient Outpatient View: OutPatientView v. 6.0. Solucient LLC, Evanston IL. 3Farwell D and Sulke N. How do we diagnose syncope? J Cardiovasc Electrophysiol. 2002;13(Supp):S9-S13. 4Olshansky B. Syncope: Overview and approach to management. In: Grubb B and Olshansky B. eds. Syncope: Mechanisms and Management. Armonk, NY:Futura;1998:15-71. 1Kenny RA, Kapoor WN. In: Benditt D, et al. eds. The Evaluation and Treatment of Syncope. Futura;2003:23-27. 2OutPatientView v. 6.0. Solucient LLC, Evanston IL. 3Farwell D, et al. J Cardiovasc Electrophysiol. 2002;13(Supp):S9-S13. 4Olshansky B. In: Grubb B and Olshansky B. eds. Syncope: Mechanisms and Management. Futura. 1998:15-71.

Impact of syncope: Quality of life 73%1 71%2 60%2 Percent of Patients 37%2 Syncope results in substantial cost to patients and to society. For example, syncope patients live with lifestyle altering restrictions that affect daily activities, mobility, and employment. Linzer M, Pontinen M, Gold DT, et al. Impairment of physical and psychological function in recurrent syncope. J Clin Epidemiol. 1991;44:1037-1043. Linzer M, Gold DT, Pontinen M, et al. Recurrent syncope as a chronic disease: Preliminary validation of a disease-specific measure of functional impairment. J Gen Int Med. 1994;9:181-186. Anxiety/ Depression Alter Daily Activities Restricted Driving Change Employment 1Linzer M. J Clin Epidemiol. 1991;44:1037. 2Linzer M. J Gen Int Med. 1994;9:181.

Syncope mortality Low mortality vs. high mortality Neurally-mediated syncope vs. syncope with a cardiac cause Soteriades ES, Evans JC, Larson MG, et al. Incidence and prognosis of syncope. N Engl J Med. 2002;347(12):878-885. [Framingham Study Population]

Diagnostic objectives Distinguish true syncope from syncope mimics Determine presence of heart disease Establish the cause of syncope with sufficient certainty to: Assess prognosis confidently Initiate effective preventive treatment

Diagnostic plan Initial Examination Monitoring Cardiac Imaging Detailed patient history Physical exam ECG Supine and upright blood pressure Monitoring Holter Event Insertable loop recorder (ILR) Cardiac Imaging Special Investigations Head-up tilt test Hemodynamics (cardiac cath) Electrophysiology study Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537. Brignole M, et al. Europace, 2004;6:467-537.

Detailed patient history Circumstances of recent event Eyewitness account of event Symptoms at onset of event Sequelae Medications Circumstances of prior events Concomitant disease, especially cardiac Pertinent family history Cardiac disease Sudden death Metabolic disorders Past medical history Neurological history Syncope The history must include detailed summary of events leading up to and following syncope events. Additionally, it is important to ascertain whether there is any evidence of underlying structural heart disease. The direction of subsequent evaluation differs in patients with and without heart disease. Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537. Raviele A, Alboni P, Sutton D, Kenny RA. Initial evaluation of the syncope patient. In: Benditt D, Blanc J-J, Brignole M, Sutton R, eds. The Evaluation and Treatment of Syncope. Elmsford, NY: Futura. 2003:38-45. Brignole M, et al. Europace, 2004;6:467-537.

Initial exam Vital signs Heart rate Orthostatic blood pressure change Cardiovascular exam: Is heart disease present? ECG: Long QT, pre-excitation, conduction system disease Echo: LV function, valve status, hypertrophic cardiomyopathy Neurological exam Carotid sinus massage Perform under clinically appropriate conditions preferably during head-up tilt test Monitor both ECG and BP HCM—Hypertrophic Cardiomyopathy Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537. Brignole M, et al. Europace, 2004;6:467-537.

Specific conditions Neurally-mediated Cardiac arrhythmia Vasovagal Syncope (VVS) Carotid Sinus Syndrome (CSS) Cardiac arrhythmia Tachy-brady syndrome Long QT syndrome Torsade de pointes Brugada syndrome Drug-induced Structural cardio-pulmonary disease Orthostatic

Neurally-mediated reflex syncope Vasovagal syncope (VVS) Carotid sinus syndrome (CSS) Situational syncope Post-micturition Cough Swallow Defecation Blood drawing, etc. The neurally-mediated reflex causes of syncope are a group of related conditions in terms of symptomatic hypotension being caused by a variable combination of bradycardia and vasodilatation. Vasovagal syncope and carotid sinus syndrome are the most frequent conditions in this group. The others occur occasionally and are usually recognized only if a detailed medical history is obtained. Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.

Vasovagal syncope Most common form of syncope 8% to 37% (mean 18%) of syncope cases Depends on population sampled Young without structural heart disase, ↑ incidence Older with structural heart disease, ↓ incidence The incidence of vasovagal syncope is poorly known. The published data that exists mostly dates from before the advent of tilt table testing. Linzer surveyed the literature and found published prevalences varying from 8% to 37% (mean 18%) of cases of syncope. Standards for diagnosis and reporting are still emerging. Linzer MD, Yang EH, Estes M, et al. Diagnosing syncope. Part 1: Value of history, physical examination, and electrocardiography. Ann Intern Med. 1997;126(12):989-996.

Tilt table test 60° - 80° Useful as diagnostic adjunct to confirm vasovagal syncope Useful in teaching patients to recognize prodromal symptoms The rationale for undertaking tilt table testing in patients suspected of having vasovagal (VVS) syncope is summarized here. The test may provide useful diagnostic information and also an opportunity for patients to become more familiar with the condition and its possible warning signs. Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537. Brignole M, et al. Europace. 2004;6:467-537.

Orthostatic hypotension Etiology Drug-induced (very common) Diuretics Vasodilators Primary autonomic failure Multiple system atrophy Parkinson’s Disease Postural Orthostatic Tachycardia Syndrome (POTS) Secondary autonomic failure Diabetes Alcohol Amyloid Orthostatic hypotension is an important cause of syncope. The medical history is usually sufficient to establish the diagnosis. However, defining the specific cause requires careful consideration of a number of important conditions. The most important conditions predisposing to orthostatic syncope are listed here. Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.

Hypersensitive carotid sinus syndrome Syncope clearly associated with carotid sinus stimulation is rare (≤1% of syncope) CSS may be an important cause of unexplained syncope/falls in older individuals Carotid sinus syndrome (CSS) is an important and often overlooked cause of syncope, and in addition is believed to be a frequent cause of unexplained falls in older individuals. The underlying cause of CSS is considered to be a hypersensitive carotid sinus. Carotid Sinus Hypersensitivity (CSH) is diagnosed by using Carotid Sinus Massage (CSM). The method of carotid sinus massage, and the findings diagnostic of CSS were presented on previous slides. Kenny RA, Richardson D, Steen N, et al. Carotid sinus syndrome: A modifiable risk factor for nonaccidental falls in older adults (SAFE PACE). J Am Coll Cardiol. 2001;38:1491-1496. Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537. Sutton R. Carotid sinus syndrome: clinical presentation, epidemiology, and natural history. In: Neurally Mediated Syncope: Pathophysiology, Investigation and Treatment. Blanc JJ, Benditt D, Sutton R. eds. Armonk, NY: Futura;1996:138. Kenny RA, et al. J Am Coll Cardiol. 2001;38:1491-1496. Brignole M, et al. Europace. 2004;6:467-537. Sutton R. In: Neurally Mediated Syncope: Pathophysiology, Investigation and Treatment. Blanc JJ, et al. eds. Armonk, NY: Futura;1996:138.

Carotid sinus massage (CSM) Method1 Massage, 5-10 seconds Don’t occlude Supine and upright posture (on tilt table) Outcome 3 second asystole and/or 50 mmHg fall in systolic BP with reproduction of symptoms = Carotid Sinus Syndrome Absolute contraindications2 Carotid bruit, known significant carotid arterial disease, previous CVA, MI last 3 months Complications Primarily neurological Less than 0.2%3 Usually transient Carotid sinus massage (CSM) is an often overlooked, yet highly cost effective test, especially in older syncope patients. CSM must be applied with care, and the method described here1 has proven both safe and effective. Note that an abnormal response to CSM (i.e., Carotid Sinus Hypersensitivity, CSH) is not diagnostic of Carotid Sinus Syndrome (CSS). Reproduction of symptoms is a crucial diagnostic element. To achieve symptom reproduction, it may be useful to conduct CSM with the patient in the upright posture. If the latter is to be done, the patient should be safely secured to a tilt table in order to prevent injury from a fall. 1Kenny RA, O’Shea D, Parry SW. The Newcastle protocols for head-up tilt table testing in the diagnosis of vasovagal syncope, carotid sinus hypersensitivity, and related disorders. Heart. 2000;83:564-569. 2Linzer M, Yang EH, Estes M, et al. Diagnosing Syncope: Part 1: Value of history, physical examination, and electrocardiography. Ann Intern Med. 1997;126(12):989-996. 3Munro N, McIntosh S, Lawson J, et al. Incidence of complications after carotid sinus massage in older patients with syncope. J Am Geriatr Soc. 1994;42:1248-1251. Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537. 1Kenny RA. Heart. 2000;83:564. 2Linzer M. Ann Intern Med. 1997;126:989. 3Munro N, et al. J Am Geriatr Soc. 1994;42:1248-1251.

Other diagnostic tests Ambulatory ECG Holter monitoring Insertable loop recorder (ILR) Tilt table test Includes drug provocation (NTG, isoproterenol) Cardiac catheterization Electrophysiology study (EPS) NTG = nitroglycerin Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537. Brignole M, et al. Europace, 2004;6:467-537.

Heart monitoring options ILR Event Recorders (non-lead and loop) Holter Monitor 12-Lead 1 day 7-30 days Up to 14 Months 10 Seconds OPTION TIME (Months) 1 2 3 4 5 6 7 8 9 10 11 12 13 14 Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537. Brignole M, et al. Europace, 2004;6:467-537.

Diagnostic yield of various tests Initial Evaluation Yield (%) History, Physical Exam, ECG, Cardiac Massage 38-40 Other Tests/Procedures Head-Up Tilt 27 External Cardiac Monitoring 5-13 Insertable Loop Recorder (ILR) 43-883-5 EP Study <2-5 Exercise Test 0.5 EEG 0.3-0.5 1Alboni P, Brignole M, Menozzi C, et al. Diagnostic value of history in patients with syncope with or without heart disease. J Am Coll Cardiol. 2001;37:1921-1928. 2Kapoor W. Evaluation and outcome of patients with syncope. Medicine. 1990;69:160-175. 3Krahn AD, Klein GJ, Yee R, et al. for the Reveal Investigators. Use of an extended monitoring strategy in patients with problematic syncope. Circulation. 1999;99;406-410. 4Krahn AD, Klein GJ, Yee R, et al. Randomized Assessment of Syncope Trial. Conventional diagnostic testing versus a prolonged monitoring strategy. Circulation. 2001;104:46-51. 5Krahn AD, Klein GJ, Yee R, et al. The high cost of syncope: Cost implications of a new insertable loop recorder in the investigation of recurrent syncope. Am Heart J. 1999;137:870-877. 6Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.

Neurological tests EEG Head CT Neurological studies (Head CT and MRI, EEG) are rarely useful in the diagnostic evaluation for syncope. Imaging may be justified if there is concern that syncope may have resulted in a head injury. Otherwise, without apparent abnormal neurological signs, such testing should be relegated to low priority. Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537. Brignole M, et al. Europace. 2004;6:467-537.

Cardiac syncope Includes cardiac arrhythmias and structural heart disease Often life-threatening Suspect if syncope exercise-induced May be warning of critical CV disease Tachy and brady arrhythmias Myocardial ischemia, aortic stenosis, pulmonary hypertension, aortic dissection Assess culprit arrhythmia or structural abnormality aggressively Initiate treatment promptly Syncope occurring as a result of cardiac arrhythmias or in association with underlying structural heart disease requires careful and aggressive evaluation. Whereas syncope in patients with normal hearts is often relatively benign, syncope in the presence of cardiac disease is often indicative of a potentially life-threatening problem. Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.

Syncope due to cardiac arrhythmias Bradyarrhythmias Sinus arrest, exit block High grade or acute complete AV block Can be accompanied by vasodilatation (VVS, CSS) Tachyarrhythmias Atrial fibrillation/flutter with rapid ventricular rate (eg, pre-excitation syndrome) Paroxysmal SVT or VT Torsade de pointes Both excessively slow as well as excessively rapid heart rates may result in sufficient drop in systemic pressure to cause syncope. In the case of tachycardias, the syncope tends to occur at the onset of the episode, before vascular constriction has an opportunity to occur. Syncope may also occur at termination of tachyarrhythmias, if a prolonged pause occurs prior to resumption of a stable rhythm. Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.

Factors contributing to sudden death likelihood Cardiovascular pathology Coronary artery disease Severe left ventricular dysfunction Cardiomyopathy Hypertrophic cardiomyopathy Arrhythmogenic right ventricular cardiomyopathy Congenital heart disease, especially coronary artery anomalies Valvular heart disease Cardiac pacemaker and conducting system disease   Hereditary channelopathies (Sudden Arrhythmic Death Syndrome (SADS)) Brugada syndrome Early repolarization syndrome (ERS) Long QT syndrome (LQTS) Short QT syndrome (SQTS) Catecholaminergic polymorphic ventricular tachycardia (CPVT)

Importance to emergency physicians Often present as recurrent syncope or brief seizures in children or young adults before sudden death occurs May have young relatives who have had sudden death ECG findings are often diagnostic Effective preventive treatment is available (ICD) Astute emergency physician may be the ONLY healthcare provider who can make the diagnosis and prevent tragic loss of a young life

Brugada syndrome Male predominance Autosomal dominant Common in Asians 40-60% prevalence of life-threatening ventricular arrhythmias and SCD Presents as syncope Downsloping ST-segment elevation in ECG leads V1–3

Early repolarization syndrome (ERS) Type I – 43% ↑ in SCD Male predominance 1-2% of adults Normalizes with exercise Type II – no ↑ in SCD

Long Q-T syndrome Hereditary Acquired causes Autosomal recessive (Jervell Lange-Nielsen syndrome) with hereditary nerve deafness Autosomal dominant (Romano Ward syndrome w/out deafness) Syncope, VF, SCD 𝑄𝑇𝑐𝑜𝑟𝑟𝑒𝑐𝑡𝑒𝑑= 𝑄𝑇𝑚𝑒𝑎𝑠𝑢𝑟𝑒𝑑 𝑅 𝑅𝑖𝑛𝑡𝑒𝑟𝑣𝑎𝑙 Bazett Formula QTc = 0.35-0.44 at HR= 60 Acquired causes Hypocalcemia Hypokalemia Hypomagnesemia Ischemia Anorexia CNS pathology QT-prolonging drugs (www.azcert.org)

Short Q-T syndrome Hereditary Acquired causes Autosomal dominant Atrial fibrillation Syncope, VF, SCD Early repolarization inferolateral leads in 65% Acquired causes Hypercalcemia Hyperkalemia Acidosis Systemic inflammatory syndrome Myocardial ischemia Increased vagal tone

Exercise-related syncope Anomalous L coronary artery off the pulmonary artery Hypertrophic cardiomyopathy Severe aortic stenosis Catecholaminergic polymorphic ventricular tachycardia Hereditary defect in myocardial calcium handling Stress-related syncope, VF, SCD ECG – unexplained sinus bradycardia at rest 50% carry a diagnosis of epilepsy before correct diagnosis established

Conclusion Syncope is a common symptom with many causes Deserves thorough investigation and appropriate treatment Clinical decision (observation) unit at VCU is an appropriate location to initiate the evaluation Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.